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Protection against myocardial ischemia-reperfusion injury in rats by a novel selective lymphotoxin binding p55TNFR / 中华急诊医学杂志
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-480743
Responsible library: WPRO
ABSTRACT
Objective To investigate the effect of a novel lymphotoxin with selectively binding to p55 tumor necrosis factor receptor (p55TNFR) on myocardial ischemia-reperfusion injury in rats in order to explore the mechanism.Methods A total of 40 SD rats were randomly (random number) assigned into four groups (n =10 in each),namely sham operation group (group A),I/R group (group B),wild type rhLTα treatment group (group C),and p55TNFR selective rhLTα (rhLTα-Q107E) treatment group (group D).After I/R model rats were established,various therapeutic agents or saline were given by continuous intravenous infusion for 24 h via a micropump.After 24 hours of treatment,serum myocardial zymogram,such as aspartate aminotransferase (AST),lactate dehydrogenase (LDH) and creatine kinase (CK),as well as superoxide dismutase (SOD),malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) activities were determined.Myocardial infarction size (MIS) was measured by nitro blue tetrazolium chloride (NBT) staining.Results Compared to sham operation group,MIS,AST,LDH,CK,MDA were increased,while the activities of SOD and GSH-Px were decreased.However,all the effects were significantly reversed by treatment with rhLTα-Q107E (P < 0.05) but not rhLTα (P > 0.05).Conclusions The rhLTα-Q107E plays a role in the protection against myocardial ischemia-reperfusion injury in rats by the mechanism of scavenging oxygen free radicals and increasing the activity of endogenous antioxidant system.

Full text: Available Database: WPRIM (Western Pacific) Type of study: Prognostic study Language: Chinese Journal: Chinese Journal of Emergency Medicine Year: 2015 Document type: Article
Full text: Available Database: WPRIM (Western Pacific) Type of study: Prognostic study Language: Chinese Journal: Chinese Journal of Emergency Medicine Year: 2015 Document type: Article
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